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. 2021 May 26;12:3176. doi: 10.1038/s41467-021-23550-w

Fig. 7. Loss of the SUN1–SPDYA interaction disrupts telomere integrity.

Fig. 7

a IF-FISH images of chromosome spreads stained for SYCP3 (green) and telomeric DNA (telC, magenta). Arrowheads indicate telomere fusions and bridges. DNA was stained by DAPI (blue). b Quantification of the number of telomere fusions and bridges per nucleus of WT (n = 30) and W151R (n = 43) spermatocytes in panel a. Red lines indicated the mean values. A two-sided Student’s t test was performed, ***P = 1.9E-24. c IF-FISH analysis of spermatocyte spreads stained for SYCP3 (green), MAJIN (red), and telomeric DNA (telC, magenta). Insets are enlarged figures of the framed regions containing telomere fusions. d Quantification of frequency of telomere fusions and bridges with (+) or without (−) MAJIN staining signal in W151R (n = 30) spermatocytes from panel c. Red lines indicated the mean values. A two-sided Student’s t test was performed, ***P = 1.4E-13. e Schematic model of the assembly of the telomere supramolecular structure at the INM. The TTM complex mediates the initial attachment of telomeres to the INM (stage 1). Association of SUN1 with the INM-anchored telomere-TTM complex stabilizes the telomere–INM connection (stage 2). Dynein-driven telomere movements allow telomeres to encounter more TTM and LINC complexes (stage 3), till the formation of the ring-shaped architecture of the supramolecular complex (stage 4), in which the TTM, the LINC, and the SPDYA–CDK2 complexes are confined into the telomere rings (bottom). Source data are provided as a Source Data file.